LncRNA NEAT1 contributes to the acquisition of a tumor like-phenotype induced by PM 2.5 in lung bronchial epithelial cells via HIF-1α activation

Jiang, Pan; Hao, Shengyu; Xie, Liang; Xiang, Guiling; Hu, Weiping; Wu, Qiao; Liu, Zilong; Li, Shanqun

doi:10.1007/s11356-021-13735-7

Cited by 18 publications

(11 citation statements)

References 33 publications

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“…In recent decades, mounting evidence has supported the idea that environmental pollutants (such as PM2.5 [ 33 , 34 , 35 ], nickel [ 36 ] and cadmium [ 37 , 38 ]) promote the malignant transformation of lung epithelial cells by changing the expression levels of ncRNAs. Dysregulation of ncRNA expression levels was also revealed to be a novel paradigm for interpretation of the toxicology of various nanoparticles [ 39 , 40 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of Candidate lncRNA and Pseudogene Biomarkers Associated with Carbon-Nanotube-Induced Malignant Transformation of Lung Cells and Prediction of Potential Preventive Drugs

Chang

Xie

et al. 2022

IJERPH

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Mounting evidence has linked carbon nanotube (CNT) exposure with malignant transformation of lungs. Long non-coding RNAs (lncRNAs) and pseudogenes are important regulators to mediate the pathogenesis of diseases, representing potential biomarkers for surveillance of lung carcinogenesis in workers exposed to CNTs and possible targets to develop preventive strategies. The aim of this study was to screen crucial lncRNAs and pseudogenes and predict preventive drugs. GSE41178 (small airway epithelial cells exposed to single- or multi-walled CNTs or dispersant control) and GSE56104 (lung epithelial cells exposed to single-walled CNTs or dispersant control) datasets were downloaded from the Gene Expression Omnibus database. Weighted correlation network analysis was performed for these two datasets, and the turquoise module was preserved and associated with CNT-induced malignant phenotypes. In total, 24 lncRNAs and 112 pseudogenes in this module were identified as differentially expressed in CNT-exposed cells compared with controls. Four lncRNAs (MEG3, ARHGAP5-AS1, LINC00174 and PVT1) and five pseudogenes (MT1JP, MT1L, RPL23AP64, ZNF826P and TMEM198B) were predicted to function by competing endogenous RNA (MEG3/RPL23AP64-hsa-miR-942-5p-CPEB2/PHF21A/BAMBI; ZNF826P-hsa-miR-23a-3p-SYNGAP1, TMEM198B-hsa-miR-15b-5p-SYNGAP1/CLU; PVT1-hsa-miR-423-5p-PSME3) or co-expression (MEG3/MT1L/ZNF826P/MT1JP-ATM; ARHGAP5-AS1-TMED10, LINC00174-NEDD4L, ARHGAP5-AS1/PVT1-NIP7; MT1L/MT1JP-SYNGAP1; MT1L/MT1JP-CLU) mechanisms. The expression levels and prognosis of all genes in the above interaction pairs were validated using lung cancer patient samples. The receiver operating characteristic curve analysis showed the combination of four lncRNAs, five pseudogenes or lncRNAs + pseudogenes were all effective for predicting lung cancer (accuracy >0.8). The comparative toxicogenomics database suggested schizandrin A, folic acid, zinc or gamma-linolenic acid may be preventive drugs by reversing the expression levels of lncRNAs or pseudogenes. In conclusion, this study highlights lncRNAs and pseudogenes as candidate diagnostic biomarkers and drug targets for CNT-induced lung cancer.

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Section: Discussionmentioning

confidence: 99%

Identification of Candidate lncRNA and Pseudogene Biomarkers Associated with Carbon-Nanotube-Induced Malignant Transformation of Lung Cells and Prediction of Potential Preventive Drugs

Chang

Xie

et al. 2022

IJERPH

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“…Ning et al [99] found 13 deregulated miRNAs related to lung cancer in the serum of mice inhaled PM 2.5 for 8 weeks. Moreover, miR-32, miR-582-5p, and miR-199a-5p participate in PM 2.5 -induced EMT and CSC processes, suggesting that miRNAs might be potential targets for lung cancer therapy [94,95,100]. We found that melatonin has an anti-tumor effect by reducing oxidative damage [101].…”

Section: Lung Cancermentioning

confidence: 70%

“…Chronic exposure to PM 2.5 can lead to the occurrence of EMT and CSC in vivo and vitro [88,92,93]. Oncogenic pathways, including Notch, Smad, HIF-1α, and PI3K/Akt pathways, have been shown to be involved in PM 2.5 -induced EMT process and facilitate tumor progression [90,92,94,95]. PM 2.5 exposure leads to genetic and epigenetic abnormalities that play prominent roles in lung carcinogenesis.…”

Section: Lung Cancermentioning

confidence: 99%

Effects of PM2.5 on Chronic Airway Diseases: A Review of Research Progress

Liu

2021

Atmosphere

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The adverse effects of polluted air on human health have been increasingly appreciated worldwide. It is estimated that outdoor air pollution is associated with the death of 4.2 million people globally each year. Accumulating epidemiological studies indicate that exposure to ambient fine particulate matter (PM2.5), one of the important air pollutants, significantly contributes to respiratory mortality and morbidity. PM2.5 causes lung damage mainly by inducing inflammatory response and oxidative stress. In this paper, we reviewed the research results of our group on the effects of PM2.5 on chronic obstructive pulmonary disease, asthma, and lung cancer. And recent research progress on epidemiological studies and potential mechanisms were also discussed. Reducing air pollution, although remaining a major challenge, is the best and most effective way to prevent the onset and progression of respiratory diseases.

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“…Furthermore, HIF-1a promotes cigarette smoke exposure-induced malignant transformation of bronchial epithelial cells, which is a process dependent on AKT/ NF-kB pathway (75). Moreover, HIF-1a also encourages epithelial-mesenchymal transition and the acquisition of cancer stem cell-like characteristics in the bronchial epithelium (76,77). Therefore, these findings indicated a link between COPD-associated airway inflammation, HIF-1a, and lung cancer.…”

Section: Hif-1a Links Copd With Lung Cancermentioning

confidence: 73%

Hypoxia-inducible factor 1-alpha is a driving mechanism linking chronic obstructive pulmonary disease to lung cancer

Wang

2022

Front. Oncol.

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Patients with chronic obstructive pulmonary disease (COPD), irrespective of their smoking history, are more likely to develop lung cancer than the general population. This is mainly because COPD is characterized by chronic persistent inflammation and hypoxia, which are the risk factors for lung cancer. However, the mechanisms underlying this observation are still unknown. Hypoxia-inducible factor 1-alpha (HIF-1α) plays an important role in the crosstalk that exists between inflammation and hypoxia. Furthermore, HIF-1α is the main regulator of somatic adaptation to hypoxia and is highly expressed in hypoxic environments. In this review, we discuss the molecular aspects of the crosstalk between hypoxia and inflammation, showing that HIF-1α is an important signaling pathway that drives COPD progression to lung cancer. Here, we also provide an overview of HIF-1α and its principal regulatory mechanisms, briefly describe HIF-1α-targeted therapy in lung cancer, and summarize substances that may be used to target HIF-1α at the level of COPD-induced inflammation.

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LncRNA NEAT1 contributes to the acquisition of a tumor like-phenotype induced by PM 2.5 in lung bronchial epithelial cells via HIF-1α activation

Cited by 18 publications

References 33 publications

Identification of Candidate lncRNA and Pseudogene Biomarkers Associated with Carbon-Nanotube-Induced Malignant Transformation of Lung Cells and Prediction of Potential Preventive Drugs

Identification of Candidate lncRNA and Pseudogene Biomarkers Associated with Carbon-Nanotube-Induced Malignant Transformation of Lung Cells and Prediction of Potential Preventive Drugs

Effects of PM2.5 on Chronic Airway Diseases: A Review of Research Progress

Hypoxia-inducible factor 1-alpha is a driving mechanism linking chronic obstructive pulmonary disease to lung cancer

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